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Visual Loss Due to Progressive Multifocal Leukoencephalopathy In CLINICOPATHOLOGIC REPORTS, CASE REPORTS, AND SMALL CASE SERIES SECTION EDITOR: W. RICHARD GREEN, MD but there was a single nucleotide visible, fine-linear white scarring in Visual Loss Due to substitution (C155T) in exon 1 of this area (Figure 2). In the most se- Progressive Multifocal the WAS gene. verely affected gyri, the cortex was Leukoencephalopathy Six weeks later his vision was bi- also involved and had a darker color, in a Congenital lateral finger counting. A magnetic with apparent expansion and soften- resonance imaging (MRI) scan ing of its affected parts. Immunodeficiency Disorder showed scattered areas of white- Although the individual le- matter foci, predominantly peri- sions were present throughout the A 20-year-old man with Wiskott- pheral and not periventricular, on cerebral hemispheres, they were Aldrich syndrome (WAS) initially de- proton density and T2-weighted most frequent bilaterally in the oc- veloped a mild visual disturbance that scans. He was given intravenous cipital poles, which were also the progressed to blindness, increasing methylprednisolone sodium succi- major site of linear cortico–white- neurological deficits, and death nate because of the possibility of de- matter junction lesions and scar- within 4 months. Wiskott-Aldrich myelination. No improvement oc- ring as well as the regions of diffuse syndrome is an X-linked immuno- curred, and he was registered as blind. cortical involvement. A microsco- deficiency disorder characterized by Reduced sensation and generalized pic examination of the brain sec- thrombocytopenia, eczema, and sus- mild weakness (level 4-5) devel- tions showed small, spherical, white ceptibility to infection.1 This case il- oped in his right-hand side and face. matter lesions that were atypical of lustrates the difficulties in reaching Reflexes were normal and he had no PML because they were associated the final diagnosis of progressive mul- dysphasia. with a considerable perivascular and tifocal leukoencephalopathy (PML) A repeat MRI scan showed an in- parenchymal inflammatory infil- in this individual and its unusual his- crease in the number of small high- trate (Figure 3). The inflamma- topathologic features. signal foci together with more con- tory infiltrate was mostly lympho- fluent areas of high signal intensity cytic in character but also contained Report of a Case. A 20-year-old and a scalloped edge in the left oc- plasma cells that were occasionally white man with WAS had a 1-month cipital region (Figure 1). Rapid de- binuclear. However, further exami- history of decline in vision. Nine terioration occurred with protracted nation indicated the presence of di- months previously, he had omitted focal seizures, total blindness, loss of agnostic enlarged magenta-colored 3 consecutive doses of immunoglob- consciousness, and death. A postmor- oligodendrocyte nuclei around the ulin, which he had been receiving tem histopathologic examination of periphery of the foci of demyelin- every 3 weeks since the age of 12 the brain revealed the papovavirus ation, containing the papovavirus years. This was restarted when he de- particles associated with PML. particles associated with PML veloped lethargy and malaise. His The fresh brain was examined (Figure 4). Other differences from mother had been diagnosed with and then prepared in slices. Tissue un- typical examples of PML were that multiple sclerosis at age 26 years. derwent light microscopic examina- the pleomorphic astrocytic reac- An ophthalmological examina- tion and was embedded in paraffin tion within the lesions was less florid tion revealed a visual acuity of 20/17 wax, sectioned, and stained with he- and that foamy macrophages were OD and 20/20 OS with normal pu- matoxylin-eosin. The brain weighed not as conspicuous, although there pillary reactions. Color vision was ab- 1570 g. External examination showed were numerous mononuclear cells normal, and visual field testing mild diffuse vascular congestion but within the larger lesions. In a few showed bilateral enlarged blind spots no focal lesions. Brain slices had large cases the isolated lesions had the with paracentral scotomata. Fundi numbers of small, gray, circular le- character of “burnt-out” lesions, appeared grossly normal. Results of sions in the white matter that were 1 with no enlarged oligodendro- fundus fluorescein angiography were to 3 mm in diameter, many of which cytes, no significant inflammatory re- unremarkable. Electrodiagnostic were close to the cortico–white- action, and a predominantly fi- evaluation was normal apart from de- matter junction. In some cases the le- brous gliosis. The linear lesions in layed visual evoked potentials, which sions were also visible within the cor- the cortico–white-matter junction were suggestive of demyelination. tical ribbon. The lesions had the had the same histological character- The patient’s biochemistry and appearance of small regions of demy- istics as the spherical lesions. The complete blood cell count were nor- elination and resembled the indi- diffuse cortical lesions showed de- mal except for a low platelet count vidual lesions of PML. In addition to myelination within the cortex and (123103/µL). Mutational analysis the spherical lesions, there were also reactive astrocytosis extending for Leber hereditary optic neuropa- irregular linear lesions along the cor- through the neuropil and around the thy and for the WAS protein gene tico–white-matter junction that in neurons, although no enlarged oli- demonstrated no Leber mutation, some instances were accompanied by godendrocyte nuclei were identi- (REPRINTED) ARCH OPHTHALMOL / VOL 119, SEP 2001 WWW.ARCHOPHTHALMOL.COM 1376 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 Figure 1. Second magnetic resonance imaging scan (17 weeks after initial Figure 2. Fresh brain slices showing large numbers of small, gray, circular symptoms) showing an increase in the number of small high signal foci with lesions in the white matter close to the cortico–white-matter junction (white more confluent areas of high signal intensity, a scalloped edge in the left arrows). Also seen are irregular linear lesions along the cortico–white-matter occipital region, and a serpiginous scalloped appearance at the gray junction (black arrowheads). matter/white matter interface involving the arcuate fibers. Figure 3. Microscopic picture showing small, spherical, white matter lesions Figure 4. Microscopic section showing the presence of diagnostic enlarged with marked vascular prominence and parenchymal infiltrate homogenous oligodendrocyte nuclei, which contain the papovavirus particles (hematoxylin-eosin, original magnification 320). associated with progressive multifocal leukoencephalopathy (arrows) at the periphery of the focus of demyelination (hematoxylin-eosin, original magnification 3100). fied within the affected regions of the hereditary optic neuropathy or the sclerosis,2 electrodiagnostic test re- cortical ribbon. possibility of a contiguous deletion in sults were was suggestive of optic the same region as the WAS gene, nerve demyelination. Visual distur- Comment. Delay in the diagnosis of leading to a phenotypic complex of bance in multiple sclerosis is almost PML was probably due to visual WAS and perhaps an X-linked cone always due to optic nerve rather than symptoms dominating this case, late dystrophy, were explored and ex- cortical involvement. The reverse is development of neurological signs, cluded. true for PML. Despite increasing cen- and the outstanding longevity and Although the lesions that ap- tral scotomata, the preserved pupil- relative good health of the patient. In- peared on the initial MRI scan were lary reflexes should have directed us herited conditions including Leber not completely typical of multiple earlier to a cortical etiology. Typical (REPRINTED) ARCH OPHTHALMOL / VOL 119, SEP 2001 WWW.ARCHOPHTHALMOL.COM 1377 ©2001 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/27/2021 PML features became more identi- At the time of referral 6 days fiable by the second MRI scan Complication From Use later, the patient’s visual acuity was (Figure 1). The histopathologic char- of Alcohol to Treat 20/200 with pinhole approxima- acteristics of this case include an un- Epithelial Ingrowth tion, and she had a large central epi- usual variant of PML: there was a thelial defect. The edematous flap After Laser-Assisted marked inflammatory response, and made the interface difficult to exam- the demyelinating lesions had an un- In Situ Keratomileusis ine. Her epithelial defect improved usual distribution. The inflamma- during the next week with conser- tory response was presumably a re- Epithelial ingrowth occurs in up to vative treatment, and her visual ac- flection of the immune status of this 4.3% of patients following laser- tivity improved to 20/80 with pin- 1 patient. Whereas most cases of PML assisted in situ keratomileusis. Treat- hole approximation. Four days later, are associated with immune sup- ment varies from observation to lift- the patient returned with 80% melt- pression, no matter what the cause, ing the flap and scraping away the ing of the flap (Figure 1). The re- this case is unusual because a epithelium. With recurrence, addi- maining nasal and temporal pieces of marked inflammatory response was tional treatment options include the the flap were removed and sent to the noted.3,4 A study of ophthalmic signs use of an excimer laser,
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